Specific malignancies associated with neurofibromatosis 1 demonstrate loss of both alleles which supports the hypothesis that NF1 acts as a tumor suppressor in some tissue. The absence of LOH (loss of heterozygosity) in benign tumors of NF1 patients suggests that the second NF1 allele may be functional. Antibody and mRNA detection of the NF1 gene product is not sensitive enough to be convincing that absence of signal loss of neurofibromin function. Identification of NF1 patients with large deletions that encompass the entire gene is the goal.